C3 Deficiency Leads to Increased Angiogenesis and Elevated Pro-Angiogenic Leukocyte Recruitment in Ischemic Muscle Tissue.
Animals
Capillaries
/ metabolism
Complement C3
/ deficiency
Disease Models, Animal
Fluorescent Antibody Technique
/ methods
Humans
Ischemia
/ genetics
Leukocytes
/ metabolism
Macrophage Activation
Macrophages
/ metabolism
Mice, Inbred C57BL
Mice, Knockout
Muscle, Skeletal
/ blood supply
Neutrophil Infiltration
Platelet Endothelial Cell Adhesion Molecule-1
/ metabolism
C3
NETs
angiogenesis
complement system
ischemia
leukocytes
macrophage polarization
macrophages
neutrophil extracellular traps
neutrophils
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
28 May 2021
28 May 2021
Historique:
received:
15
04
2021
revised:
26
05
2021
accepted:
27
05
2021
entrez:
2
6
2021
pubmed:
3
6
2021
medline:
22
6
2021
Statut:
epublish
Résumé
The complement system is a potent inflammatory trigger, activator, and chemoattractant for leukocytes, which play a crucial role in promoting angiogenesis. However, little information is available about the influence of the complement system on angiogenesis in ischemic muscle tissue. To address this topic and analyze the impact of the complement system on angiogenesis, we induced muscle ischemia in complement factor C3 deficient (C3-/-) and wildtype control mice by femoral artery ligation (FAL). At 24 h and 7 days after FAL, we isolated the ischemic gastrocnemius muscles and investigated them by means of (immuno-)histological analyses. C3-/- mice showed elevated ischemic damage 7 days after FAL, as evidenced by H&E staining. In addition, angiogenesis was increased in C3-/- mice, as demonstrated by increased capillary/muscle fiber ratio and increased proliferating endothelial cells (CD31
Identifiants
pubmed: 34071589
pii: ijms22115800
doi: 10.3390/ijms22115800
pmc: PMC8198161
pii:
doi:
Substances chimiques
Complement C3
0
Platelet Endothelial Cell Adhesion Molecule-1
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Deutsche Forschungsgemeinschaft
ID : SFB 914 Z01
Organisme : Münchner Universitätsgesellschaft
ID : 10278
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